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Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) signalling pathways are involved in a vast array of cellular events and are often altered in human cancers. This Review discusses how studies in mouse models have contributed to our understanding of the functions of these pathways in different cancers, and the implications for therapeutic approaches.
The PI3K–Akt pathway is vital to the growth and survival of cancer cells and consequently inhibitors targeting this pathway are entering clinical trials. What is the therapeutic potential of such drugs and what might the challenges and limitations be?
The human tumour suppressor LKB1 directly phosphorylates and activates AMPK, a central metabolic sensor. AMPK is a key therapeutic target in patients with diabetes, and the connection between AMPK and several tumour suppressors suggests that therapeutic manipulation of this pathway using established diabetes drugs warrants investigation in patients with cancer.
The pharmacological activity of tamoxifen is dependent on metabolic conversion by the enzyme cytochrome P450 2D6 (CYP2D6). This Review discusses the existing data that relateCYP2D6 genotypes to tamoxifen response. Can the analysis of CYP2D6genotype be used to optimize breast cancer therapy?
This Opinion article focuses on the multilevel crosstalk between the Notch pathway and the p53 and p63 pathways. can selective or combined targeting of these pathways improve the efficacy and reduce the toxicity of cancer therapies?
A major challenge exists in assessing the risk of developing cancer from exposures to low-dose radiation — which are encountered during diagnostic scans, for example. What factors influence low-dose cancer risk and what might this mean for current protection measures?
